Figure 4C–E shows that the reduction of cardiomyocyte size could be responsible for the mitigation of cardiac hypertrophy in the AAV9-CNPase/TAAC group. The left ventricular section in the pressure overload-induced group was characterized by an excessive accumulation and a disrupted composition of extracellular matrix proteins, wherein the AAV9-CNPase administration trimmed the fibrosis response (Figure 4F,G). This evidence concerns the gene CNP and cardiac hypertrophy.